Necrotizing sialometaplasia

Necrotizing Sialometaplasia

A rare condition in which there is ulceration usually in a smoker in the palate,which heals spontaneously over several weeks.Association with salivary gland infractions.histology can be confusing,since it has been appearance resembling neoplasia(Pseudo epitheliomatous hyperplasia)

· Affects mainly minor glands of the palate

· Painless,ulcerated swelling,the margins are irregular and heaped up or everted.

· Chronic inflammation in the minor salivary glands and necrosis of acini

· Duct tissues undergoes squamous metaplasia and proliferates to produce a pseudomembranous appearance

Sjogren's syndrome

Sjogren's Syndrome

· Assosiation of dryness of the mouth of dryness of the eyes(+rheumatoid arthritis)

Primary Sjogrens syndrome(Sicca syndrome)

· Dry mouth+Dry eyes , not associated with any connective tissue disease

Secondary Sjogrens syndrome

· Dry mouth+Dry eyes , associated with rheumatoid arthritis or other connective tissue disease

Oral effects of sjogrens syndrome

· Discomfort

· Difficulties with eating and swallowing

· Disturbed taste sensation

· Disturbed quality of speech

· Predisposition to infection

Clinical features

· In established cases oral mucosa often dry,red,shiny,parchment like

· Tongue-typically red,atrophic papillae,dorsum of the tongue become lobulated coblestone appearance

· Candidal infections are common

· Later generalized erythema of the mucosa occur

· Infective suppurative parotitis may occur

Occular effects of sjogrens syndrome

· Failure of tear secretion

· Failure of clearance of foreign particles from the cornea and conjunctiva(keratoconjinctivitis sicca)

· Griity sensation of the eyes and inflammation

· Risk of impairment or loss of sight

Aetiology & Pathology

· Autoimmune disease

· The disease is systemic and affects all exocrine glands including those of the skin,vagina,lung and pancreas.

· Lymphocytes(CD4) infiltrate the glands and cluster around duct replacing acinar cells

· Progressive destruction of secretory acini

· Proliferation of some duct tissues as epimyoepithelial islands(myoepithelial syeloadenitis)

· Finally destruction of acini and replacement of the whole gland by dense lymphocytic infiltrate

· Auto antibodies-Salivary duct antibodies,Rheumatoid factor,SS-A,SS-B,Rheumatoid arthritis precipitin

Chronic sialadenitis

Chronic sialadenitis

· Usually a complication of duct obstrution

· Usually unilateral and asympomaic or with intermittant painful swelling of the gland

Pathology

· There are varying degrees of destruction of acini,duct dilatation,Chronic inflammatory cell infiltration predominantly lymphoplasmacytic

· Extensive interstitial fibrosis and squamous cell metaplasia in duct epithelium

· Calculus formation may be seen in dilated ducts

Dental caries and diseases

Dental caries is the most prevalent chronic disease

Classification

• Histopathologically-Enamal caries,Dentine caries,Cementum caries
• Clinically(according to location)-Pit and fissure,Smooth surface
• Clinial cause-Chronic,Acute

Smooth surface caries

• On approximal surface
• Early white spot lesion
• Then brown/black-due to pigmentation by dietary or bacterial products
• In SEM –cocci attached,small rounded dipressions and rough areas seen.
• Early lesions are conical in shape and 4 zones are seen.
• Translucent zone-due to demineralization
• Dark zone-due to remineralization
• Body of the lesion-due to greatest demineralization(subsurface decalcification)
• Surface zone-greater resistant to cariesactivity,30-40 micrometeres.relatively unaffected.
• Body-with water immersion with polarized microscope+bifringence-yellowcolour
• Surface zone-By a microradiograph
• Dark zone-with quinolne

Pit and fissure caries

• Cone shaped
• Base towards EDJ-because of this shape more dentinal tubules involved
• Occlusal surface caries(ground sec.-cz if demineralised 95% of inorganic part looses)
• Pit and fissure caries
• With steep walls and narrow bases easily cause caries
• In microradiograph lesion appear as radiolucent dark demineralised area
• In tooth-caries fissure is dark brown
• No loss of enamel surface continuity
• Morphology is intact
• Lesion can spread along DEJ
• Form cone shaped lesion in dentine
• With only small penetration of enamel is a common finding

Caries of dentine

• Caries of dentine(decalcified sec.-cz less inorganic part than enamel-so retain considerable amount after decalcification)
• After cavity forms in enamel carious process spreads along DEJ-rapid involvement of dentinal tubules-form- cone shaped lesion,apex towards pulp
• Dentine caries can occur as a result of exposure of dentine due to abrasion
• In ground section dentine show,
• pigmented zone
• Dark zone
• transparent zone-highly mineralized(radioopaque)deposition of ca2+salts in dentinal tubules to seal against bacteria.
• Decalcified section
• small amount on the surface of lesion
• involve deeper dentinal tubules-darkly stained
• initial decalcification of tubular walls-distention of tubules by placing microbes-focal areas of liquifraction necrosis form within dentinal tubules.those foci are filled with necrotic debris andd numerous microbes
• toward surface complete loss of dentine structure
• clefts parallel to contour lines of dentine(filled with necrotic debris + microbes)

Root caries

• After gingival recession
• Cementum is attached,readily decalcified
• Cementum softens beneth plaque over a wide area-cause soucer shaped cavity
• Underline dentine soon involved
• Cemnentum invade along sharpy’s fibers
• Infection spread belween lamelle along incremental lines-dentine split up and progressively destroy by demineralization and liquiofraction

Pulpitis

• Open –chronic hyperplastic pulpitis
• Closed –acute closed,chronic closed

Acute closed pulpitis

• Initial hyperemia limited to area underneath irritant.infiltration by inflammatory cells-destruction of odontoblasts & adjacent mesenchyme followed.
• Limited area of necrosis-form minute abscess localized by granulation tissue-inflammation spread until all pulp-entire pulp has been destroyed and replaced by inflammatory cells and dilated vessels

Chronic closed pulpitis

• Mononuclear cells infiltration
• More vigorus connective tissue reaction
• Small area of pulpal necrosis and pus formation is localized by well defined wall of granulation tissue-minute abscess form
• Reminder of pulp may appear normal
• Rarely inflammation is well localized beneth the exposure by-partial calcific barriersr benerth lesion(in X-ray dentine bridges) or reactionary dentine.
• Such changes likely to follow up pulp capping
• Calcific barriers usually poor-inflammation spread beneth but in successful reactionary entine-complete barrier-preserve rest of pulp.
• Open pulpitis
• Occationally pulp servives but chronically inflamed beneth wide exposure despite wide infection believed to be assiociate dwith open apices which allow adequate bld supply

Chronic Hyperplastic pulpitis(pulp polyp)

• Rarely despite of exposure and heavy infection.pulp not merely survive but proliferate through opening
• Clinically dusky red/pinkish soft nodule protruding in to cavity
• May tender/bleed on probing
• Histologically-odontoblasts survive,pulp replaced by granulation tissue,as mass grow out to cavity-it can become epithelialized and coverd by layer of well formed SSE
• Protects mass
• Subside

Branchial cyst

Branchial Cyst

· Arising from branchial arch remnants

· it has also been called lymphoepithelial cyst suggesting it's origin from cystic transformation of epithelium entrapted in cervical lymphnodes

· BC originated from 2nd arch->lateral aspect of upper neck near anterior border of sernocledomastoid muscle or at the mandibular angle

· Lesion->circumscribed fluctuent mass

· Young adults no sexual prediction

· Small ones canbe found in the floor of the mouth,Clinically resembles mucous retention cysts

· lined by stratified squamous epithelium

· Occationally columnar or cuboidal

· Cyst wall is composed of lymphoid tissue with scattered germinal centre surrounded by CT.